The renal actions of nitrendipine and its influence on the neural regulation of calcium and sodium reabsorption in the rat.

Infusion of nitrendipine at 0.5 micrograms/kg/min into pentobarbitone-anaesthetized rats with either intact or sectioned renal nerves did not change renal blood flow or glomerular filtration rate, but in both groups it significantly increased urine flow between 80 and 100%, calcium excretion between 85 and 130%, absolute sodium excretion between 105 and 140% and fractional sodium excretion by 80 to 105%. Administration of nitrendipine at 1.0 micrograms/kg/min into intact and renally denervated rats decreased blood pressure by 18-20 mm Hg, had no effect on renal haemodynamics, and caused significant increases in urine flow, calcium excretion, and absolute and fractional sodium excretions of identical magnitude observed with the lower dose of nitrendipine. Low-frequency renal nerve stimulation did not change either blood flow or glomerular filtration, but it significantly decreased urine flow by 27%, calcium excretion by 35%, and absolute and fractional sodium excretions by 32 and 36%, respectively. The magnitude and pattern of these responses to renal nerve stimulation were not altered in the presence of either dose of nitrendipine. These results suggest that nitrendipine directly inhibits the tubular reabsorption of calcium and sodium, but that this drug does not interfere with the adrenergic regulation of the reabsorption of these ions.